Regulation of The Tumor Suppressor Activity of P53 In Human Breast Cancer

1999 ◽  
Author(s):  
James J. Manfredi
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Suppressor Activity ◽  
Tumor Suppressor Activity

scholarly journals Tumor Suppressor Activity of Klotho in Breast Cancer Is Revealed by Structure–Function Analysis

2015 ◽  
Vol 13 (10) ◽  
pp. 1398-1407 ◽  
Author(s):  
Hagai Ligumsky ◽  
Tami Rubinek ◽  
Keren Merenbakh-Lamin ◽  
Adva Yeheskel ◽  
Rotem Sertchook ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Structure Function ◽  
Function Analysis ◽  
Suppressor Activity ◽  
Tumor Suppressor Activity

scholarly journals ECRG4 acts as a tumor suppressor gene frequently hypermethylated in human breast cancer

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Gao-Yan Tang ◽  
Guo-Jun Tang ◽  
Lu Yin ◽  
Chen Chao ◽  
Ren Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Human Breast Cancer ◽  
Suppressor Gene ◽  
Human Breast ◽  
Cancer Related Gene ◽  
And Migration ◽  
Gene 4

Abstract Human breast cancer is a malignant form of tumor with a relatively high mortality rate. Although esophageal cancer-related gene 4 (ECRG4) is thought to be a possible potent tumor suppressor gene that acts to suppress breast cancer, its precise role in this disease is not understood. Herein, we assess the correlation between ECRG4 expression and DNA methylation, probing the potential epigenetic regulation of ECRG4 in breast cancer. We analyzed ECRG4 promoter methylation via methylation-specific PCR (MSPCR), bisulfite sequencing, and a promoter reporter assay in human breast cancer cell lines and samples. Gene expression was assessed by quantitative real-time PCR (qPCR), while protein levels were assessed by Western blotting. CCK8 assays were used to quantify cell growth; Esophageal cancer-related gene 4 wound healing assays were used to assess cellular migration, while flow cytometry was used to assess apoptosis and cell cycle progression. Apoptosome formation was validated via CO-IP and Western blotting. We found that human breast cancer samples exhibited increased methylation of the ECRG4 promoter and decreased ECRG4 expression. Remarkably, the down-regulation of ECRG4 was highly associated with promoter methylation, and its expression could be re-activated via 5-aza-2′-deoxycytidine treatment to induce demethylation. ECRG4 overexpression impaired breast cancer cell proliferation and migration, and led to G0/G1 cell cycle phase arrest. Moreover, ECRG4 induced the formation of the Cytc/Apaf-1/caspase-9 apoptosome and promoted breast cancer cell apoptosis. ECRG4 is silenced in human breast cancer cells and cell lines, likely owing to promoter hypermethylation. ECRG4 may act as a tumor suppressor, inhibiting proliferation and migration, inducing G0/G1 phase arrest and apoptosis via the mitochondrial apoptotic pathway.

Epigenetic silencing of the tumor suppressor klotho in human breast cancer

2011 ◽  
Vol 133 (2) ◽  
pp. 649-657 ◽  
Author(s):  
Tami Rubinek ◽  
Michal Shulman ◽  
Shira Israeli ◽  
Shikha Bose ◽  
Ayelet Avraham ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Human Breast Cancer ◽  
Epigenetic Silencing ◽  
Human Breast
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